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Bio 111 > Chapter 22 > Flashcards

Chapter 22 Flashcards

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Biology 101 flashcards
1
Q

Pathogens

A

harmful disease causing agents

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2
Q

Bacteria

A

-Single celled
-composed of prokaryotic cells

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3
Q

Virsues

A

Not cells they are very small and contain DNA and RNA in protein capsules and must enter a cell

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4
Q

Fungi

A

composed of eukaryotic cells that have a cell wall external to the plasma membrane

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5
Q

Protozoans

A

microscopic unicellular eurkaryotic
organisms that lack a cell wall
-Intra or extracellular
-This enters the blood

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6
Q

Prions

A

small fragments of proteins that cause disease in nervous tissue

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7
Q

Innate immunity

A

-what you are born with. IT provides multiple components that protect against a wide array of substances

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8
Q

1st line of defence

A

Skin and mucosal membrane (prevent entry)

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9
Q

2nd line of defence

A

Nonspecific internal defenses
-Immune response (ex macrophages, NK cells)
-Chemical (inferno or complement)
-Physiologic responses (inflammation)
-Plasma membrane

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10
Q

Skin

A

-1st defense
-Physical barrier of epidermis & dermis
-Sweat & sebaceous glands release antimicrobials
-importance evident with burn victim

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11
Q

Mucous membrane

A

-line body openings
-Mucus and antimicrobial secretions (Defensins, lysozyme, IgA , acid)
-Various other mechanisms and secretions in different body areas (cilia and resp)

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12
Q

Defensins

A

small cysteine-rich cationic proteins across cellular life, including vertebrate and invertebrate animals, plants, and fungi. They are host defense peptides, with members displaying either direct antimicrobial activity, immune signaling activities, or both.

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13
Q

lysozyme

A

protein present in many mucosal secretions (tears, saliva, and mucus) and tissues of animals and plants, and plays an important role in the innate immunity, providing protection against bacteria, viruses, and fungi.

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14
Q

Selected immunity

A
  1. Phagocytes (neutrophils, macrophages, dendritic cells)
    Apoptosis-initiating (NK cell)
    Parasite-destroying (eosinophils)
    Proinflammatory chemical-secreting (basophils, mast cells)
  2. Inflammation
  3. Antimicrobial proteins (inferons)
  4. Fever
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15
Q

Phagocytes include

A

-Dendritic cell
-infectious agent engulfed
-Macrophages
-Phagosomes
-Lysosomes
-Phagolysomes destroy infectious agent
-They engulf foreign substances

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16
Q

Dendritic cells

A

Antigen presenting cells that phagocytose pathogens & display antigens on their surface that are recognized by T cells (adaptive)

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17
Q

Selected Immune cells: NK cells

A

Circulate in blood and accumulate in 2nd lymphoid structures

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18
Q

Selected immune cells: parasite destroying

A

Degranulate & release cytotoxic chemicals that create pores in parasite cells

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19
Q

Selected immune cells: Pro-inflammatory chemical secreting

A

-Chemical alarm
-Vasodilation goes up, local blood flow goes up
-FLuid clotting factors exudate
-Increased movement of fluid from blood to injury tissue
-Increased chemotaxis to attract immune cell decrease inflammation

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20
Q

Chemotaxis

A

Refers to the directional migration of cells in response to chemical gradients

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21
Q

Histamine source

A

mascells and basophil granules

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22
Q

Histamine physiological effects

A

Vasodilation of local arterioles = increased blood flow
Permeability of local capillaries = increased exudate (fluid with clotting factors & antibodies)
Chemotaxis of leukocytes

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23
Q

Prostaglandins, leukotrienes source

A

Produced from a component in all cell membranes by actions of neutrophils, basophils & others

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24
Q

Prostaglandins, leukotrienes effect

A

Vasodilation of local arterioles = increased blood flow
Permeability of local capillaries = increased exudate (fluid with clotting factors & antibodies)
Chemotaxis of leukocytes and increased pain

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25
Q

kinins (bradykinin) source

A

Precursor protein is cut by enzyme in saliva, plasma, urine & neutrophils to become active kinins

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26
Q

Kinins effect

A

Vasodilation of local arterioles = increased blood flow
Permeability of local capillaries = increased exudate (fluid with clotting factors & antibodies)
Chemotaxis of leukocyte and increased daub and chemotaxis creates more kinins

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27
Q

Complement proteins source

A

Blood

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28
Q

Complement protein effect

A

O-ICE:
Opsonization increases phagocytosis
Intensifies inflammation
Cytolysis lyses pathogens
Elimination of antibody complexes aids in the adaptive immune response

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29
Q

Cytokines (see slide 46 for details)
Interferons (IFNs)
Interleukins (ILs)
Colony-stimulating factors (CSFs)
Tumor necrosis factors (TNFs)
(source)

A

Many cells including T-cells, dendritic cells & macrophages

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30
Q

Cytokines (see slide 46 for details)
Interferons (IFNs)
Interleukins (ILs)
Colony-stimulating factors (CSFs)
Tumor necrosis factors (TNFs)

A

Enhances inflammation
Mainly involved in cell-mediated (T-cell) adaptive immunity

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31
Q

Four cardinal signs of Inflammation

A

Redness: increased blood flow
Heat: Increased blood flow and metabolic activity
Swelling: Increase fluid loss from capillaries to tissue
Pain: Pro-inflammatory chemical activation of complement and compression due to increased fluid

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32
Q

CAM

A

Cell adhesion molecules

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33
Q

Inflammation step 1

A
  1. release of inflammatory and chemotactic factors
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34
Q

Inflammation step 2

A

Vascular changes
-vasodilation of arterioles
-increase in capillary permeability
-Display of CAMS

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35
Q

Inflammation step 3

A

Recruitment of leukocytes
-magination
-Diapendesis
-chemotaxis
Stick, squeeze, scoot
Fluid clotting

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36
Q

Antimicrobial proteins: Complient system

A

Increase inflammation, elimination of immune capsule, opsonization, cytolysis

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37
Q

How does Increased inflammation happen

A

Mast cells, basophils, neutrophils and macrophages

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38
Q

What is the purpose of a fever

A

-mobilizes defences accelerates repairs inhibits pathogens
-Increased metabolic rate to speed healing
-Inhibit bacterial growth

39
Q

Levels of fever

A

Low-grade: 38-38.3oC
Intermediate grade: 38.8oC
High-grade: 39.4-40oC;
Dangerous high-grade: >40oC

40
Q

T Lymphocytes

A

Effective against antigens within cells regulate antigen presenting cells

41
Q

Cytotoxic T Lymphocytes

A

involved in directly killing intracellular pathogens and eliminating mutated and cancerous cells

42
Q

B lymphocytes

A

(provide antibody mediated immunity) effective antigen outside cells does not require antigen presenting cells

43
Q

Adaptive vs Innate

A

Adaptive has
1. Specificity (response to Ag)
2. Uses lymphocytes (Many different lymphocytes each specific for particular ag)
3. has memory (activation, clones, memory, fast)
4. Is systemic (not restricted to site of injury circulation in blood lymph

44
Q

Antigens are

A

self generating
Any substances that can mobilize adaptive defenses
Usually a protein or large polysaccharide not normally found in the body

45
Q

Foreign antigens

A

bind immune components (Different from body molecules)

46
Q

Self antigens

A

Do not bind immune components
(Own nodes molecule)

47
Q

Autoimmune disorder

A

Immune system reacts self as if it was foreign

48
Q

Immunogenicity

A

ability of an antigen to trigger lymphocyte proliferation (multiplication)

49
Q

Hapten

A

small molecule that cannot be an antigen on its own, bind to self protein become immunogenic and harmful

50
Q

Antigenic determinant

A

-also known as an epitope= specific site on antigen recognized by receptors on immune cells.
-Each has a different shape
-Pathogens can have multiple determinants
-can be recognized by many antibodies

51
Q

Self-Antigens & Major Histocompatibility (MHC) Proteins

A

MHC proteins are one of many that identify a cell as self
-have genetically determined structure that is unique to individual
-MHCs can bind either a self or foreign antigen & display it on the cell surface

52
Q

Lymphocytes Life cycle

A
  1. formation
  2. Maturation
  3. seeding
  4. Antigen encounter and activation
  5. Proliferation and differentiation
52
Q

Who does T cells bind to

A

T-cells can only bind antigens that are presented to them on MHC proteins

53
Q

Lymphocyte Maturation

A

-Educated as they mature
-Immunocomptence becomes able to recognize one specific antigen
-Self tolerance is unresponsive to self antigens

54
Q

Lymphocyte Formation

A

B & T-cells originate in red bone marrow

55
Q

Lymphocyte Seeding (colonization)

A

Immunocompetent, naïve B & T-cells seed the 2nd lymphoid
-circulate to increase chance that they will find their antigen

56
Q

Antigen encounter and activation

A

Antigen binding selects that cell for further development = clonal selection
-activation if signal are present

57
Q

Lymphocyte proliferation and differentiation

A

-Lymphocytes multiply rapidly once activated making identical clones of itself
-Most become effector lymphocytes and do the work
-Some become memory lymphocytes and circulate constantly “patrol”

58
Q

Antigen Presenting cells (APCs)

A

Dendrite, macrophages, B lymphocytes

59
Q

Dendrite cells

A

Found at body’s frontiers
Internalize pathogens & migrate to Lymphnodes
Most important way of ensuring T-cells encounter antigens

60
Q

Macrophages

A

-there is a wide distribution they engulf and eliminate infected cells

61
Q

B-Lymphocytes

A

-Cannot activate naive T cells
-Can only present to helper Cells to assist in their own activation

62
Q

Humoral Immunity Primary response

A

100 000 receptor cells
activated B cells
Plasma cells (effector B)
Secreted antibodies
antigens binds to receptors on V cell
Proliferation to form clots
Memory B cells primed to respond to same antigen

63
Q

Humoral secondary response

A

(could be years later)
Clone of the cell indexical to ancestor
Subsequent challenges by same antigen results in large fast response

64
Q

Active Immunity

A

-Production of memory cells due to contact with antigens

64
Q

Primary and Secondary Response

A

Primary: 3-6 days activation, proliferation, differentiation into plasma cell
Secondary: Lower (shorter) lag time due to memory B cells

65
Q

Naturally Acquired active immunity

A

-Direct exposure to antigen following entry of the pathogens into the body naturally

66
Q

Articfically acquired Active immunity

A

Antigen exposure from vaccine

67
Q

Passive immunity

A

-No production of memory cells, antibodies from another person or an animal

68
Q

Naturally acquired passive immunity

A

transfer is mother to child across the placenta or breast milk

69
Q

Artificially acquired passive immunity

A

Transfer of serum containing antibody from another person or animal (Rabies vaccine, snake venom antibodies)

70
Q

Antibody

A

immunoglobulin (Ig) proteins produced against a specific, soluble antigen (i.e., those in the blood & lymph)

71
Q

Antibody structure

A

4 polypeptide chains
Variable region, constant region,

72
Q

Immunoglobulin classes

A

IgM, IgA, IgD, IgG, IgE (MADGE)

73
Q

IgM

A

(pentamer)
B-cell antigen receptor

First antibody produced during primary response

Readily activates complement

Potent agglutinating agent

Only fetal antibody

74
Q

IgA

A

Secretory IgA in body secretions – sweat, saliva, intestinal juice, milk

Stops pathogens from attaching to mucous membranes & epidermis
(DIMER)

75
Q

IgD

A

Monomer
(B cell antigen receptor)

76
Q

IgG

A

Monomer
Most abundant antibody in plasma (75-85%)

Main antibody of secondary response

Readily activates complement

Can cross placenta – passive immunity to fetus

77
Q

IgE

A

Monomer
Stem binds to mast cells & basophils

Antigen binding triggers release of chemicals from granules – histamine etc.

Levels rise during severe allergic reactions

78
Q

Neutrolization

A

Antibody covers biologically active portion of microbe or toxin

79
Q

Agglutination

A

(elimination of bacteria) Antibody cross-link cells forming a clump. Easier for phagocytes to see and eat

80
Q

Precipitation

A

Antibody cross-links circulating particles forming an insoluble antigen-antibody complex

81
Q

Antibody targets and functions

A

Antigen-antibody complexes inactivate targets & tag them for elimination by innate immune and adaptive system
-3 are due to Antigen-antibody binding
-3 are due to exposure of Fc region after antigen-antibody binding
-

82
Q

Opsonization

A

Fc region of antibody binds to receptors of phagocytes cell triggering phagocytosis

83
Q

Complement fixation

A

Fc region of antibody binds complement proteins complement is activated

84
Q

Activation of NK cells

A

Fc region of antibody binds to an NK cell, triggering release of cytotoxic chemicals

85
Q

Types of T cells and function

A

CD4 Helper Cell (Th)
-Helps activate B cells, Cells, macrophages, innate immune system
-Releasing cytokines
(don’t fear If any villain dare invade I will come to the rescue)
and
CD8 Cytotoxic (killer) T cell (Tc) Kill apoptosis perforin granzymes (find and kill)

86
Q

Major categories of Cytokines

A

Interleukin, Tumor necrosis factor, Colony stimulating factor, interferon
Released from one cell & bind to receptors of target cells
Cell that released it (autocrine)
Local cells (paracrine)
Distant cells after circulating through blood (endocrine)
Have short half-life

87
Q

Interleukin (IL)

A

-regulates immune cells, T-lymphocytes, macrophages, endothelial cells and other various cells
-IL followed by a number

88
Q

Tumor necrosis factor (TNF)

A

Destroys tumour cells, T-Lymphocytes, macrophages, mast cells, dendritic cells
TNF followed by a greek letter

89
Q

Colony stimulating factor

A

Stimulates leukopoesis in bone marrow to increase synthesis of a specific type of leukocytes
first letter and then followed by CSF

90
Q

Inferons

A

Interferes with replication of pathogens that enter cells
-infected cell, NK cells, T-Lymphocytes
-IFN followed by a greek letter

91
Q

Response of CD4 Helper Lymphocyte

A
  1. first signal CD4 binds with MHC class II molecule of APCc, TCR interacts with antigen within MHC class II molecule
    -Activated helper T Lymphocytes form a clone of activated and memory helper T Lymphocytes
    IL 2 released from helper TLymphocutes bind to promote proliferation

Bio 111 (4 decks)

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